Abstract

Endothelial cells (EC) are attractive targets for gene therapy because they can deliver therapeutic proteins both locally and systemically. Helper-dependent adenoviral (HDAd) vectors are useful for EC-targeted gene therapy because they efficiently transduce EC and express transgenes persistently in vivo. However, obtaining high-level and stable in vivo expression from HDAd is a challenge. Our current goal of transducing EC with HDAd to treat atherosclerosis will likely require high-level, stable expression of atheroprotective genes such as apolipoprotein A-I (apoA-I) and interleukin-10 (IL-10).

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